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      Angiotensin-Converting Enzyme Inhibitors as a Risk Factor for Contrast-Induced Nephropathy

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          Background/Aims: The aim of the present study was to assess the influence of chronic angiotensin-converting enzyme (ACE) inhibitor administration on the development of contrast-induced nephropathy (CIN) in patients undergoing coronary angiography. Methods: A total of 230 patients with renal insufficiency and age ≧65 years were divided into two groups according to prior use of ACE inhibitors (ACE inhibitor group, n = 109; control group, n = 121). CIN was defined as an increase of ≧25% in creatinine over the baseline value within 48 h of angiography. Results: CIN occurred in 17 patients (15.6%) in the ACE inhibitor group and 7 patients (5.8%) in the control group (p = 0.015). Serum creatinine level increased from 1.34 ± 0.20 to 1.53 ± 0.27 mg/dl in the ACE inhibitor group and from 1.33 ± 0.18 to 1.45 ± 0.19 mg/dl in the control group (p < 0.001). Chronic ACE inhibitor administration was a risk indicator of CIN [odds ratio 3.37; 95% confidence interval 1.14–9.94; p = 0.028]. Multi-vessel coronary involvement (p = 0.001), hypoalbuminemia (p = 0.005), diabetes mellitus (p = 0.006), GFR ≤40 ml/min (p = 0.010), and congestive heart failure (p = 0.024) were other risk indicators of CIN. Conclusion: Chronic ACE inhibitor administration is a risk for developing CIN in elderly patients with renal insufficiency.

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          Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention.

          In patients undergoing percutaneous coronary intervention (PCI) in the modern era, the incidence and prognostic implications of acute renal failure (ARF) are unknown. With a retrospective analysis of the Mayo Clinic PCI registry, we determined the incidence of, risk factors for, and prognostic implications of ARF (defined as an increase in serum creatinine [Cr] >0.5 mg/dL from baseline) after PCI. Of 7586 patients, 254 (3.3%) experienced ARF. Among patients with baseline Cr 2.0, all had a significant risk of ARF. In multivariate analysis, ARF was associated with baseline serum Cr, acute myocardial infarction, shock, and volume of contrast medium administered. Twenty-two percent of patients with ARF died during the index hospitalization compared with only 1.4% of patients without ARF (P 2.0 are at high risk for ARF. ARF was highly correlated with death during the index hospitalization and after dismissal.
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            Pathophysiology of contrast medium-induced nephropathy.

            Contrast medium-induced nephropathy (CIN) is a well-known cause of acute renal failure, but the development of CIN remains poorly understood. A number of studies have been performed with the one aim, to shed some light onto the pathophysiology of CIN. These have led to manifold interpretations and sometimes contradicting conclusions. This review critically surveys mechanisms believed to mediate CIN by highlighting the complex pathophysiologic entity, including altered rheologic properties, perturbation of renal hemodynamics, regional hypoxia, auto- and paracrine factors [adenosine, endothelin, and reactive oxygen species (ROS)], and direct cytotoxic effects. Moreover, the importance of physicochemical properties of contrast media are made clear. The more recently developed iso-osmolar contrast media are dimers, not monomers as the widely used nonionic low osmolar contrast media. The dimers have physicochemical features different from other contrast media which may be of clinical importance, not only with respect to osmolality. The viscosity of the commercially available dimers is considerably higher than blood. Many experimental studies provide evidence for a greater perturbation in renal functions by dimeric contrast media in comparison to nonionic monomeric contrast media. Clinical trials have yielded conflicting results.
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              The renin-angiotensin-aldosterone system and the kidney: effects on kidney disease.

              The renin-angiotensin-aldosterone system regulates renal vasomotor activity, maintains optimal salt and water homeostasis, and controls tissue growth in the kidney. However, pathologic consequences can result from overactivity of this cascade, involving it in the pathophysiology of kidney disease. An activated renin-angiotensin-aldosterone system promotes both systemic and glomerular capillary hypertension, which can induce hemodynamic injury to the vascular endothelium and glomerulus. In addition, direct profibrotic and proinflammatory actions of angiotensin II and aldosterone may also promote kidney damage. The majority of the untoward effects associated with angiotensin II appear to be mediated through its binding to the angiotensin II type 1 receptor. Aldosterone can also induce renal injury by binding to its receptor in the kidney. An understanding of this system is important to appreciate that inhibitors of this cascade can reduce the progression of chronic kidney disease in proteinuric disease states. Pharmacologic agents that can interfere with this cascade include angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aldosterone receptor antagonists. This paper will provide an overview of the renin-angiotensin system, review its role in kidney disease, examine the renal effects of inhibition of this cascade in experimental animal models, and review clinical studies utilizing renin-angiotensin-aldosterone inhibitors in patients with diabetic and nondiabetic nephropathies.

                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                August 2006
                26 May 2006
                : 104
                : 1
                : c20-c27
                Departments of aNephrology, bFirst Cardiology, and cRadiology, Ataturk Training and Research Hospital, Izmir, Turkey; dDepartment of Medicine, Division of Nephrology, Vanderbilt University Medical Center, Nashville, Tenn., USA
                93255 Nephron Clin Pract 2006;104:c20–c27
                © 2006 S. Karger AG, Basel

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                Figures: 3, Tables: 3, References: 29, Pages: 1
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